• Int J Med Sci · Jan 2014

    Cyanidin 3-O-glucoside reduces Helicobacter pylori VacA-induced cell death of gastric KATO III cells through inhibition of the SecA pathway.

    • Sa-Hyun Kim, Hyunjun Woo, Min Park, Ki-Jong Rhee, Cheol Moon, Dongsup Lee, Woo Duck Seo, and Jong Bae Kim.
    • 1. Department of Clinical Laboratory Science, Semyung University, Jaecheon 390-711, Republic of Korea;
    • Int J Med Sci. 2014 Jan 1; 11 (7): 742-7.

    AbstractTwo key virulence factors of Helicobacter pylori are the secreted virulent proteins of vacuolating toxin A (VacA) and cytotoxin associated protein A (CagA) which lead to damages of gastric epithelial cells. We previously identified that the cyanidin 3-O-glucoside (C3G) inhibits the secretion of both VacA and CagA. In the current report, we show that C3G inhibits VacA secretion in a dose-dependent manner by inhibiting secretion system subunit protein A (SecA) synthesis. As SecA is involved in translocation of bacterial proteins, we predicted that inhibition of the SecA pathway by C3G should decrease H. pylori-induced cell death. To test this hypothesis, the human gastric cell line KATO III cells were co-cultured with H. pylori 60190 (VacA(+)/CagA(+)) and C3G. We found that C3G treatment caused a decrease in activation of the pro-apoptotic proteins caspase-3/-8 in H. pylori-infected cells leading to a decrease in cell death. Our data suggest that consumption of foods containing anthocyanin may be beneficial in reducing cell damage due to H. pylori infection.

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